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Researchers from St. Jude Children’s Research Hospital have discovered that inhibiting an enzyme called cyclin-dependent kinase 2 (CDK2) protects mice and rats from noise- or drug-induced hearing loss. The study, which will be published March 7 in the Journal of Experimental Medicine, suggests that CDK2 inhibitors prevent the death of inner ear cells, which has the potential to save the hearing of millions of people around the world.

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Researchers in France have discovered that, though a tattoo may be forever, the skin cells that carry the tattoo pigment are not. Instead, the researchers say, the cells can pass on the pigment to new cells when they die. The study, which will be published March 6 in the Journal of Experimental Medicine, suggests ways to improve the ability of laser surgery to remove unwanted tattoos.

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A team of researchers from the Cleveland Clinic Lerner Research Institute have found that gradually depleting an enzyme called BACE1 completely reverses the formation of amyloid plaques in the brains of mice with Alzheimer’s disease, thereby improving the animals’ cognitive function. The study, which will be published February 14 in the Journal of Experimental Medicine, raises hopes that drugs targeting this enzyme will be able to successfully treat Alzheimer’s disease in humans.

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Houston Methodist researchers have a new explanation for what causes the lungs’ airways to close during asthma attacks. The researchers who published the study in the Feb. 5 issue of the Journal of Experimental Medicine note that the discovery holds promise for developing a new class of drugs different from the steroids currently used to treat asthma.

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An international team of researchers led from Karolinska Institutet have, in experiments on mice, pinpointed a mechanism for the conversion of energy-storing white fat into energy-expending brown fat. The study is published in the Journal of Experimental Medicine.

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A team of researchers in Italy and Austria has determined that a drug approved to treat chronic lymphocytic leukemia (CLL) may be less effective in a particular subset of patients. The study, which will be published January 4 in the Journal of Experimental Medicine, reveals that ibrutinib has a diminished capacity to delocalize and kill tumor cells expressing an adhesive protein called CD49d, but combining ibrutinib treatment with drugs that block CD49d activation could prevent the tumor cells from sheltering in lymphoid organs.

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Researchers at the University of Pennsylvania have discovered how the Pacific midshipman fish can hum continuously for up to an hour in order to attract potential mates. The study, which is featured on the cover of the January 2018 issue of the Journal of General Physiology, explains how the muscle fibers surrounding the fish’s swimbladder can sustain the high rates of contraction—up to 100 times per second—that are needed to produce the animal’s distinctive call.

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Researchers in Italy have discovered how specific versions of a protein called Numb protect the key tumor suppressor p53 from destruction. The study, which will be published December 21 in the Journal of Cell Biology, suggests that the loss of these particular Numb proteins makes breast cancers more aggressive and resistant to chemotherapy, but points the way toward new therapeutic approaches that could improve patient outcome by preserving p53 levels.

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Genentech researchers have identified an enzyme that shifts pancreatic cancer cells to a more aggressive, drug-resistant state by epigenetically modifying the cells’ chromatin. The study, which will be published December 11 in the Journal of Cell Biology, suggests that targeting this enzyme could make pancreatic cancer cells more vulnerable to existing therapies that currently have only limited effect against this deadly form of cancer.

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Researchers from Harvard Medical School and the Institute of Systems Biology have discovered that the remains of tumor cells killed by chemotherapy or other cancer treatments can actually stimulate tumor growth by inducing an inflammatory reaction. The study, which will be published November 30 in The Journal of Experimental Medicine, also reveals that a family of molecules called resolvins can suppress this unwanted inflammatory response, suggesting new ways to enhance the effectiveness of existing cancer therapies.

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Researchers in Germany have demonstrated that hematopoietic stem cell (HSC) transplants can be improved by treatments that temporarily prevent the stem cells from dying. The approach, which is described in a paper to be published September 7 in The Journal of Experimental Medicine, could allow those in need of such transplants, including leukemia and lymphoma patients, to be treated with fewer donor stem cells while limiting potential adverse side effects.

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Recent outbreaks of Zika virus have revealed that the virus causes brain defects in unborn children. But in a study to be published September 5 in The Journal of Experimental Medicine, researchers from Washington University School of Medicine in St. Louis and the University of California, San Diego report that the virus could eventually be used to target and kill cancer cells in the brain.

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Researchers from Yale University School of Medicine have discovered that defects in the transport of lysosomes within neurons promote the buildup of protein aggregates in the brains of mice with Alzheimer’s disease. The study, which will be published August 7 in The Journal of Cell Biology, suggests that developing ways to restore lysosome transport could represent a new therapeutic approach to treating the neurodegenerative disorder.

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Researchers from McGovern Medical School at The University of Texas Health Science Center at Houston have discovered that the symptoms of diabetes can be induced by a misfolded form of a pancreatic protein. The findings, which are reported in a paper to be published August 1 in The Journal of Experimental Medicine, raise the possibility that type 2 diabetes can be transmitted by a mechanism similar to prion diseases such as Creutzfeldt-Jakob disease or Bovine Spongiform Encephalopathy (mad cow disease).

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An international team of scientists has developed a method to rapidly produce specific human antibodies in the laboratory. The technique, which will be described in a paper to be published July 24 in The Journal of Experimental Medicine, could speed the production of antibodies to treat a wide range of diseases and facilitate the development of new vaccines.

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Researchers from the University of Colorado School of Medicine have discovered that a process that protects the body from autoimmune disease also prevents the immune system from generating antibodies that can neutralize the HIV-1 virus. The findings, which will be published July 11 in The Journal of Experimental Medicine, might be considered by scientists trying to develop a vaccine that can stimulate the production of these neutralizing antibodies.

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Researchers from The Ohio State University have discovered how blows to the head cause numerous small swellings along the length of neuronal axons. The study, “Polarity of varicosity initiation in central neuron mechanosensation,” which will be published June 12 in The Journal of Cell Biology, observes the swelling process in live cultured neurons and could lead to new ways of limiting the symptoms associated with concussive brain injuries.

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Researchers at Memorial Sloan Kettering Cancer Center in New York have discovered that bacteria living in the gut provide a first line of defense against severe Listeria infections. The study, which will be published June 6 in The Journal of Experimental Medicine, suggests that providing these bacteria in the form of probiotics could protect individuals who are particularly susceptible to Listeria, including pregnant women and cancer patients undergoing chemotherapy.

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Researchers in Japan have identified a receptor protein on the surface of heart cells that promotes chronic heart failure. The study, “Corticotropin releasing hormone receptor 2 exacerbates chronic cardiac dysfunction,” which will be published May 26 in The Journal of Experimental Medicine, suggests that inhibiting this protein could help treat a disease that affects more than 20 million people worldwide.

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An international team of researchers has discovered that a microRNA produced by certain white blood cells can prevent excessive inflammation in the intestine. The study, “Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome,” which will be published May 9 in The Journal of Experimental Medicine, shows that synthetic versions of this microRNA can reduce intestinal inflammation in mice and suggests a new therapeutic approach to treating patients with Crohn’s disease or ulcerative colitis.

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Researchers at the University of Maryland have identified how the pathogenic bacterium Pseudomonas aeruginosa uses tension-activated membrane channels to stop itself from swelling up and bursting when it is suddenly exposed to water. The study, which will be published April 19 in The Journal of General Physiology, helps explain how this bacterium—a major cause of hospital-acquired infections—persists in a variety of different environments.

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Researchers in France have developed a new method that will allow doctors to detect minute amounts of a protein called interferon- in patient samples. The technique, which is described in the study “Detection of interferon- protein reveals differential levels and cellular sources in disease” published April 18 in The Journal of Experimental Medicine, will aid the diagnosis and treatment of numerous autoimmune diseases, including systemic lupus erythematosus (SLE) and dermatomyositis.

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Researchers from Harvard Medical School have discovered that the body’s immune system initially detects the presence of anthrax spores by recognizing RNA molecules that coat the spores’ surface. But this prompts an unfavorable immune response that hinders the body’s fight against anthrax once the spores have germinated into live bacteria, according to the study “TLR sensing of bacterial spore-associated RNA triggers host immune responses with detrimental effects,” which will be published April 11 in The Journal of Experimental Medicine.

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Researchers in Germany have developed a transgenic mouse that could help scientists identify new influenza virus strains with the potential to cause a global pandemic. The mouse is described in a study, “In vivo evasion of MxA by avian influenza viruses requires human signature in the viral nucleoprotein,” that will be published April 10 in The Journal of Experimental Medicine.

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Researchers at Bascom Palmer Eye Institute, part of the University of Miami Miller School of Medicine, have identified a new molecule that induces the formation of abnormal blood vessels in the eyes of diabetic mice. The study, “Secretogranin III as a disease-associated ligand for antiangiogenic therapy of diabetic retinopathy,” which will be published March 22 in The Journal of Experimental Medicine, suggests that inhibiting this molecule may prevent similarly aberrant blood vessels from damaging the vision of not only diabetics, but also premature infants.

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Researchers in China have discovered that a metabolic enzyme called AKR1B1 drives an aggressive type of breast cancer. The study, “AKR1B1 promotes basal-like breast cancer progression by a positive feedback loop that activates the EMT program,” which has been published in The Journal of Experimental Medicine, suggests that an inhibitor of this enzyme currently used to treat diabetes patients could be an effective therapy for this frequently deadly form of cancer.

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Researchers in Germany have discovered that a tumor suppressor protein thought to prevent acute myeloid leukemia (AML) can actually promote a particularly deadly form of the disease. The study, “RUNX1 cooperates with FLT3-ITD to induce leukemia,” which will be published online February 17 in The Journal of Experimental Medicine, suggests that targeting this protein could be an effective treatment for certain AML patients.

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Researchers at Cold Spring Harbor Laboratory in New York have discovered that a protein called Importin-11 protects the anti-cancer protein PTEN from destruction by transporting it into the cell nucleus. The study, “The nuclear transport receptor Importin-11 is a tumor suppressor that maintains PTEN protein,” which will be published online February 13 in The Journal of Cell Biology, suggests that the loss of Importin-11 may destabilize PTEN, leading to the development of lung, prostate, and other cancers.

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Boston Children’s Hospital researchers have uncovered a new molecular pathway that inhibits the myelination of neurons in the brains of patients with the rare genetic disorder tuberous sclerosis complex (TSC). The study, “Neuronal CTGF/CCN2 negatively regulates myelination in a mouse model of tuberous sclerosis complex,” which will be published online February 9 in The Journal of Experimental Medicine, suggests new ways to treat some of the neurological symptoms associated with TSC, including autism and epilepsy.

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Researchers from the Chinese Academy of Sciences have discovered that the metabolic enzyme phosphoglycerate mutase 1 (PGAM1) helps cancer cells repair their DNA and found that inhibiting PGAM1 sensitizes tumors to the cancer drug Olaparib (Lynparza). Their findings in the study “Phosphoglycerate mutase 1 regulates dNTP pool and promotes homologous recombination repair in cancer cells,” which has been published in The Journal of Cell Biology, suggest that this FDA-approved ovarian cancer medicine has the potential to treat a wider range of cancer types than currently indicated.

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Defects in the body’s regulatory T cells cause inflammation and autoimmune disease by altering the type of bacteria living in the gut, researchers from the University of Texas Health Science Center at Houston have discovered. The study, which will be published online December 19 in The Journal of Experimental Medicine, suggests that replacing the missing gut bacteria, or restoring a key metabolite called inosine, could help treat children with a rare and often fatal autoimmune disease called IPEX syndrome.

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Researchers have discovered that mice with Huntington’s disease (HD) suffer defects in muscle maturation that may explain some symptoms of the disorder. The study, “Progressive Cl− channel defects reveal disrupted skeletal muscle maturation in R6/2 Huntington’s mice,” which will be published online November 29 in The Journal of General Physiology, suggests that HD is a disease of muscle tissue as well as a neurodegenerative disorder and that therapies targeting skeletal muscle may improve patients’ motor function.

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Conventional, high-dose chemotherapy treatments can cause the fibroblast cells surrounding tumors to secrete proteins that promote the tumors’ recurrence in more aggressive forms, researchers have discovered. Frequent, low-dose chemotherapy regimens avoid this effect and may therefore be more effective at treating certain types of breast and pancreatic cancer, according to the murine study “Metronomic chemotherapy prevents therapy-induced stromal activation and induction of tumor-initiating cells,” which will be published online November 23 in The Journal of Experimental Medicine.

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Researchers from the University of Toronto have discovered that mice infected with the common gut parasite Tritrichomonas muris are at an increased risk of developing inflammatory colitis. Their findings, which have been published online in The Journal of Experimental Medicine, expand the type of gut-resident microorganism that can affect the health of their host and suggest that related parasites may cause gastrointestinal disease in humans.

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Researchers at Stanford University School of Medicine have identified several new biological markers to measure the progression of the inherited neurodegenerative disorder Huntington’s disease. Their findings, which will be published online November 7 ahead of issue in The Journal of Experimental Medicine, could benefit clinical trials that test new treatments for the disease.

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Researchers in Japan have discovered that the adrenergic nervous system controls when white blood cells circulate through the body, boosting the immune response by retaining T and B cells in lymph nodes at the time of day when they are most likely to encounter foreign antigens. The study, “Adrenergic control of the adaptive immune response by diurnal lymphocyte recirculation through lymph nodes,” will be published online October 31 ahead of issue in The Journal of Experimental Medicine.

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Researchers in France have identified a molecular motor that controls the release of inflammatory factors that cause severe and fatal allergic reactions. The study, “Kinesin-1 controls mast cell degranulation and anaphylaxis through PI3K-dependent recruitment to the granular Slp3/Rab27b complex,” which will be published online October 24 ahead of issue in The Journal of Cell Biology, suggests that targeting this motor may be a new way to treat patients undergoing anaphylactic shock.

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Researchers from The Ohio State University have discovered that spinal cord injury alters the type of bacteria living in the gut and that these changes can exacerbate the extent of neurological damage and impair recovery of function. The study, “Gut dysbiosis impairs recovery after spinal cord injury,” by Kristina A. Kigerl et al., which will be published online October 17 ahead of issue in The Journal of Experimental Medicine, suggests that counteracting these changes with probiotics could aid patients’ recovery from spinal cord injuries.

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Researchers have discovered that an enzyme called uracil-DNA glycosylase (UNG) protects the ends of B cell chromosomes to facilitate the proliferation of these antibody-producing cells in response to infection. The study “UNG protects B cells from AID-induced telomere loss,” which will be published online October 3 ahead of issue in The Journal of Experimental Medicine, also suggests that targeting this enzyme may help treat certain types of non-Hodgkin’s lymphoma.

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Researchers have built a three-dimensional map of the anthrax toxin that may explain how it efficiently transfers its lethal components into the cytoplasm of infected cells. The study, “Structure of anthrax lethal toxin prepore complex suggests a pathway for efficient cell entry,” which will be published online September 26 ahead of print in The Journal of General Physiology, suggests that the bacterial protein acts as a “conveyer belt” that allows toxic enzymes to continuously stream across cell membranes.

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Mice placed on a low-calorie diet are less likely to develop abdominal aortic aneurysms, according to a new study in The Journal of Experimental Medicine. The paper, “Calorie restriction protects against experimental abdominal aortic aneurysms in mice,” which will be published online September 26 ahead of issue, suggests new ways to prevent the often fatal condition from occurring in humans.

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Researchers have discovered that secondary infection with the Methicillin-resistant Staphylococcus aureus (MRSA) bacterium (or “superbug”) often kills influenza patients because the flu virus alters the antibacterial response of white blood cells, causing them to damage the patients’ lungs instead of destroying the bacterium. The study, which will be published online August 15 ahead of issue in The Journal of Experimental Medicine, suggests that inhibiting this response may help treat patients infected with both the flu virus and MRSA.

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Scientists in Germany have developed a new approach that may prevent leukemia and lymphoma patients from developing graft-versus-host disease (GvHD) after therapeutic bone marrow transplants. The researchers describe the successful application of their strategy in mice in “Exogenous TNFR2 activation protects from acute GvHD via host T reg cell expansion,” which will be published online August 15 ahead of issue in The Journal of Experimental Medicine.

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A team of Israeli researchers has discovered that mutations in STN1, a gene that helps maintain the ends of chromosomes, cause the rare, inherited disorder Coats plus syndrome. The study, “Mutations in STN1 cause Coats plus syndrome and are associated with genomic and telomere defects,” will be published online ahead of issue July 18 in The Journal of Experimental Medicine.

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A team of New York-based researchers has compared the effects of two disease-causing mutations, potentially explaining why patients with the rare genetic disorder keratitis-ichthyosis-deafness (KID) syndrome can experience different sets of symptoms. The study, “Syndromic deafness mutations at Asn 14 differentially alter open stability of Cx26 hemichannels,” will be published online June 27 in The Journal of General Physiology.

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Michel C. Nussenzweig has won the 2016 Robert Koch Award, one of Germany’s most prestigious scientific prizes, honoring extraordinary accomplishments in infectious disease research. Nussenzweig will share the €100,000 prize with Alberto Mantovani of Humanitas University for their achievements in immunology.

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Researchers at the National Institute of Neurological Disorders and Stroke have discovered that boosting the transport of mitochondria along neuronal axons enhances the ability of mouse nerve cells to repair themselves after injury. The study, “Facilitation of axon regeneration by enhancing mitochondrial transport and rescuing energy deficits,” which has been published in The Journal of Cell Biology, suggests potential new strategies to stimulate the regrowth of human neurons damaged by injury or disease.

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Researchers from University College London have discovered that the widely used antiinflammatory drug HUMIRA doesn’t just work by inhibiting its target protein, TNF, but by enhancing a particular function of TNF in rheumatoid arthritis patients. The study, “Anti-TNF drives regulatory T cell expansion by paradoxically promoting membrane TNF–TNF-RII binding in rheumatoid arthritis,” which will be published online June 6 in The Journal of Experimental Medicine, may help explain the divergent efficacies of different TNF-targeting drugs.

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Oncologists at the Fred Hutchinson Cancer Research Center have successfully treated a patient with metastatic melanoma by combining two different types of immunotherapy. Cassian Yee and colleagues describe their approach in a paper, “Combined IL-21–primed polyclonal CTL plus CTLA4 blockade controls refractory metastatic melanoma in a patient,” that will be published online May 30 in The Journal of Experimental Medicine.

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Researchers at the Spanish National Center for Cardiovascular Research have discovered that the ends of heart muscle cell chromosomes rapidly erode after birth, limiting the cells’ ability to proliferate and replace damaged heart tissue. The study, “Postnatal telomere dysfunction induces cardiomyocyte cell-cycle arrest through p21 activation,” which will be published online May 30 in The Journal of Cell Biology, suggests potential new interventions to boost the heart’s capacity to repair itself after a heart attack.